ALT-711 (thiazolium chloride), 15g

ALT-711 (thiazolium chloride), 15g

Brand: Full Catalog
Product Code: AT11
In Stock
Price: $87.00


Alagebrium, formerly called ALT-711 and also known as thiazolium chloride, belongs to a class of research chemicals designed to break advanced glycation end-products (AGEs).  AGEs are formed during glycation, which is when a glucose molecule bonds to a lipid molecule.  AGEs form naturally in the body during metabolism and eliminate slowly; over time and especially in old age AGEs can accumulate and cause stiffening of artery walls, neuropathy of the peripheral nervous system, retinal damage, pancreatic beta-cell damage.  AGEs may be implicated in other chronic diseases found in the elderly, such as Alzheimer’s. 

Alagebrium is no longer in development; however, many studies found benefits, such as the following data as summed up by Guo et al:

To investigate the possible effects of alagebrium chloride (ALT-711) on oxidative stress (OS) process in aging hearts, we examined the role of ALT-711 in cardiac function and OS in the heart of aging rats. Increased mitochondrial DNA (mtDNA) deletion as well as nearly a twofold increase in advanced glycation end products (AGEs) accumulation were observed in aging heart, whereas only about 50% of the superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities were seen. However, after treatment with ALT-711, preserved cardiac diastolic function accompanied with reduced mtDNA deletion and about 30% of AGEs decrease was observed in aging hearts. In addition, ALT-711 can increase SOD and GSH-PX activities in aging hearts as well as in cultured cardiomyocytes. In conclusion, our study suggests that AGEs accumulation and the abnormalities in the OS in aging hearts can be attenuated by ALT-711, and this might be a novel underlying mechanism for ALT-711 in the treatment of cardiovascular diseases that develop with aging.[1]

Advanced glycation endproducts are implicated in diabetes-related complications; alagebrium may be of therapeutic use in reversing this damage:

The biochemical process of advanced glycation appears to play a central role in the development and progression of diabetic vascular complications. A number of strategies to influence this pathway have been designed, one of which involves the putative advanced glycation end-product (AGE) crosslink breaker, alagebrium which has been shown in in vitro studies to cleave preformed AGE crosslinks. This agent has been studied in various models of diabetic complications and has been shown to attenuate diabetic renal disease, cardiac dysfunction, and atherosclerosis. In addition to the ability of alagebrium to reduce tissue levels of AGEs, this drug appears to inhibit activation of certain protein kinase C isoforms. Planned clinical studies in diabetic subjects at risk of complications should assist in determining the role of alagebrium in the prevention, retardation, and reversal of diabetic micro- and macrovascular disease.[2]

The effects of AGEs are profound; Semba et al posit that alagebrium may be a useful addition to other strategies, such as avoiding dietary AGEs found in highly processed foods:

We conducted a review of the scientific literature on the relationship of advanced glycation end products (AGEs) with aging. AGEs are a heterogeneous group of bioactive molecules that are formed by the nonenzymatic glycation of proteins, lipids, and nucleic acids.

Humans are exposed to AGEs produced in the body, especially in individuals with abnormal glucose metabolism, and AGEs ingested in foods. AGEs cause widespread damage to tissues through upregulation of inflammation and cross-linking of collagen and other proteins. AGEs have been shown to adversely affect virtually all cells, tissues, and organ systems. Recent epidemiological studies demonstrate that elevated circulating AGEs are associated with increased risk of developing many chronic diseases that disproportionally affect older individuals…Based on these data, we propose that accumulation of AGEs accelerate the multisystem functional decline that occurs with aging, and therefore contribute to the aging phenotype. Exposure to AGEs can be reduced by restriction of dietary intake of AGEs and drug treatment with AGE inhibitors and AGE breakers. Modification of intake and circulating levels of AGEs may be a possible strategy to promote health in old age, especially because most Western foods are processed at high temperature and are rich in AGEs.[3]

Tikellis et al compared mice fed a Western-based diet high in fats and processed with a lower-fat diet, and as a third variable randomly treated some mice in a double-blind fashion with alagebrium, ultimately concluding alagebrium is a promising agent for reversing the cardiac damage induced by such habits:

A Western diet was associated with cardiac hypertrophy, inflammation, mitochondrial-dependent superoxide production, and cardiac AGE accumulation in wild-type mice. Although RAGE-KO mice fed a Western diet also became obese and accumulated intramyocardial lipid, cardiomyocyte hypertrophy, inflammation, and oxidative stress were attenuated compared with wild-type mice. Similarly, mice of both strains receiving alagebrium chloride had reduced levels of inflammation and oxidative stress, in association with a reduction in cardiac AGEs and RAGE. This study suggests that AGEs represent important mediators of cardiac injury associated with a Western fast-food diet. These data point to the potential utility of AGE-reducing strategies in the prevention and management of cardiac disease.[4]

Please see this link to an interesting study on how ALT-711 and sildenafil may have emiliorative effects on erectile dysfunction:


[1] Guo Y, Lu M, Qian J, Cheng YL. Alagebrium chloride protects the heart against oxidative stress in aging rats. J Gerontol A Biol Sci Med Sci. 2009 Jun;64(6):629-35. Epub 2009 Mar 18.

[2] Coughlan MT, Forbes JM, Cooper ME. Role of the AGE crosslink breaker, alagebrium, as a renoprotective agent in diabetes.  Kidney Int Suppl. 2007 Aug;(106):S54-60.

[3] Semba RD, Nicklett EJ, Ferrucci L. Does accumulation of advanced glycation end products contribute to the aging phenotype? J Gerontol A Biol Sci Med Sci. 2010 Sep;65(9):963-75. Epub 2010 May 17.

[4] Tikellis C, Thomas MC, Harcourt BE, Coughlan MT, Pete J, Bialkowski K, Tan A, Bierhaus A, Cooper ME, Forbes JM. Cardiac inflammation associated with a Western diet is mediated via activation of RAGE by AGEs. Am J Physiol Endocrinol Metab. 2008 Aug;295(2):E323-30. Epub 2008 May 13.


*The latter article is intended for educational / informational purposes only. THIS PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. Bodily introduction of any kind into humans or animals is strictly forbidden by law.


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